Background

In the United States, the incidence of closed head injury is estimated to be approximately 200 cases per 100,000 persons per year. In a population of 291.6 million people, this rate equates to more than 570,000 patients annually. Approximately 15% of these patients succumb to the injury upon arrival to the emergency department.
[1, 2, 3, 4, 5, 6, 7, 8]

Traumatic injuries remain the leading cause of death in children and in adults aged 45 years or younger. Head injuries cause immediate death in 25% of acute traumatic injuries.
[9] Traumatic brain injury (TBI) results in more deaths than does trauma to other specific body regions.
[10] Penetrating intracranial injuries have worse outcomes than closed head injuries.
[11] Motor vehicle collisions (MVCs) are the most common cause of closed head injuries for teenagers and young adults.
[12] Alcohol or drug use contributes to as many of 38% of cases of severe head trauma in younger patients.
[13] A recent development has been the apparent increase in brain injuries among the elderly; this increase is thought to be related to the use of anticoagulant and antiplatelet drugs.
[14]

Head injury significantly contributes to deaths from trauma.
[7] Annual mortality from closed head injuries is approximately 100,000 patients or 0%, 7%, and 36% of mild, moderate, and severe head injuries, respectively.
[7, 9] Patients with severe head injury have a 30-50% mortality rate, and those who survive are often left with severe neurological deficits that may include a persistent vegetative state.
[9] Permanent disability in survivors ranges from 10-100%, depending on the severity of the injuries. This produces more than 90,000 newly disabled patients annually, including 2500 who are in a persistent vegetative state.
[7, 9]

The financial burden of head injuries in the United States is estimated to be $75-100 billion annually.
[15] Injuries to the central nervous system tend to be the most costly on a per-patient basis because they often result in debilitating physical, psychological, and psychosocial deficits that, in turn, require extensive long-term rehabilitation and care.

The last 3 decades have been alternately exhilarating and frustrating for clinicians and researchers interested in TBI. Laboratory and bedside research has greatly improved our understanding of posttraumatic cerebral pathophysiology. These new insights have failed to make the transition to clinically used therapies. Many of the major clinical trials of the last decades have been negative studies that have shown us what does not work. Demonstrating the efficacy of new treatments has been extraordinarily difficult.
[16]

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Pathophysiology

Closed head injuries are classified as either primary or secondary. A primary injury results from the initial anatomical and physiological insult, which is usually direct trauma to the head, regardless of cause. A secondary injury results from hypotension, hypoxia, acidosis, edema, or other subsequent factors that can secondarily damage brain tissue (see Secondary injuries). Free radicals are thought to contribute to these secondary insults, especially during ischemia.

Primary injuries

Cerebral concussion is defined as an altered mental state that may or may not include loss of consciousness that occurs as a result of head trauma. Concussion is also known as mild traumatic brain injury (MTBI). The American Academy of Neurology grading scale is widely used to categorize the degree of concussions.

Concussion symptoms or mental status change resolves in 15 min or less

Concussion symptoms or mental status change resolves in more than 15 min

...

Sport-related concussions are frequent, with 300,000 cases reported each year.
[17] Football players and boxers are particularly exposed to repetitive concussions, leading to the condition now known as chronic traumatic encephalopathy syndrome. Repetitive concussions may result in chronic subclinical motor dysfunctions linked to intracortical inhibitory system abnormalities.
[18] Parkinsonian cognitive decline due to strionigral degeneration is now a well-known consequence of repetitive concussions; cumulative diffuse axonal injury effects in the midbrain are due to increased vulnerability to shear forces in that region. Increasing a player’s neck strength may be an effective way to minimize the risk of future concussions, as studies with Hybrid III dummies seem to indicate.
[19]

Cerebral contusion

Cerebral contusions are commonly seen in the frontal and temporal lobes. They may accompany skull fracture, the so-called fracture contusion. The most worrisome trait of these contusions is their tendency to expand. This usually occurs from 24 hours to as long as 7-10 days after the initial injury. For this reason, cerebral contusions are often followed with a repeat head CT scan within 24 hours after injury.

Coup injuries (contusions) are caused by direct transmission of impact energy through the skull into the underlying brain and occur directly below the site of injury. Contrecoup injuries are caused by rotational shear and other indirect forces that occur contralateral to the primary injury. Rotational force causes the basal frontal and temporal cortices to impact or sweep across rigid aspects of the skull, the sphenoid wing, and petrous ridges. Delayed enlargement of traumatic intraparenchymal contusions and hematomas is the most common cause of clinical deterioration and death. However, progression of contusion is highly variable, and although most remain unchanged for days, a few enlarge, some quite rapidly.

In a retrospective study, well-known prognostic factors were found to predict contusion enlargement. The strongest prognostic factor is the presence of traumatic subarachnoid hemorrhage. The size of the intraparenchymal hemorrhage means that large lesions are probably in an active phase of progression at the time of the initial CT scan. The concurrent presence of a subdural hematoma was also predictive. Clinical features, such as the initial Glasgow Coma Score (GCS; see the Glasgow Coma Scale calculator) and intracranial pressure (ICP), were not predictive of progression. The ideal time for a rescan is unclear, although most of the growth seems to occur within the first 24 hours of injury.
[20]

Epidural hematoma

The incidence of epidural hematomas is 1% of all head trauma admissions, as depicted in the image below.
[21] Epidural hematomas most commonly (85%) result from bleeding in the middle meningeal artery. Epidural hematomas, however, may occur in locations other than in the distribution of the middle meningeal artery. Such hematomas may develop from bleeding from diploic vessels injured by overlying skull fractures.
[9] Epidural hematomas are often associated with a "lucid interval," a period of consciousness between states of unconsciousness. The lucent period is presumed to end when the hematoma expands to the point that the brainstem is compromised.

The most common surgical intracranial lesion is a subdural hematoma. These occur in approximately 20-40% of patients with severe injuries, as depicted in the image below.
[13, 22] A surface or bridging vessel (venous) can be torn because the brain parenchyma moves during violent head motion. The resulting bleeding causes a hematoma to form in the potential space between the dural and arachnoid. A lucid interval is less likely to develop in this type of injury than in epidural hematomas. Subdural hematomas can be the result of an arterial rupture as well; these hematomas have the peculiar location in the temporoparietal region and differ in form from those caused by the bridging vein rupture, which typically rupture in the frontoparietal parasagittal region. Hematoma thickness and the midline shift of the brain are often analyzed; when the midline shift exceeds the hematoma thickness (positive displacement factor), a poorer prognosis has been found.
[23]

An intraventricular hemorrhage is another intracerebral lesion that often accompanies other intracranial hemorrhages, as depicted in the image below. Intraventricular blood is an indicator of more severe head trauma. Intraventricular blood also predisposes the patient to posttraumatic hydrocephalus and intracranial hypertension, which may warrant placement of an intraventricular catheter (if emergent drainage needed) or ventriculoperitoneal shunt for chronic hydrocephalus.

Despite the absence of any intracranial mass lesion or history of hypoxia, some patients remain unconscious after a TBI. Brain MRI studies have demonstrated a clear correlation between white matter lesions and impairment of consciousness after injury. The deeper the white matter lesion, the more profound and persistent the impairment of consciousness.
[24]

The usual cause for persistent impairment of consciousness is the condition referred to as diffuse axonal injury, as depicted in the image below. Approximately 30-40% of individuals who die from TBI reveal postmortem evidence of DAI and ischemia.
[25] This type of injury commonly results from traumatic rotation of the head, with mechanical forces that act on the long axons, leading to axonal structural failure. DAI is caused by an acceleration injury and not by contact injury alone. The brain is relatively incompressible and does not tolerate tensile or shear strains well. Slow application of strain is better tolerated than rapid strain. The brain is most susceptible to lateral rotation and tolerates sagittal movements best.
[26]

MRI of the brain that shows diffuse axonal injury (DAI) and hyperintense signal in the corpus callosum (splenium), septum pellucidum, and right external capsule.

Recent studies suggest that the magnitude of rotational acceleration needed to produce DAI requires the head to strike an object or surface. These factors also increase the likelihood that DAI will be accompanied by other intracranial lesions.
[26] These mechanical forces physically dissect these axons into proximal and distal segments. If a sufficient number of axons are involved, profound neurologic deficits and unconsciousness may ensue.

These same forces may act on the cerebral circulation, causing disruption of vessels and various forms of micro–intracerebral hemorrhages and macro–intracerebral hemorrhages, including Duret hemorrhages, which are commonly lethal when they occur in the brainstem. Duret hemorrhages of the midbrain and pons are small punctate hemorrhages that are often caused by arteriole stretching during the primary injury, as depicted in the image below. They may also result during transtentorial herniation as a secondary injury when arterial perforators are compressed or stretched.

MRI of the brain (sagittal view) that shows a Duret hemorrhage in the splenium of the corpus callosum.

The major focus in the management of acute closed head injury is the prevention of secondary injuries and the preservation of neurological functions that are not damaged by the primary injury.

Posttraumatic vasospasm can be a cause of ischemic damage after severe traumatic brain injury, with parenchymal contusions and fever being risk factors. Diffuse mechanical injury and activation of inflammatory pathways may be secondary mechanisms for this vasospasm. Patients with parenchymal contusions and fever may benefit from additional screening.
[29]

Cerebral ischemia

Cerebral ischemia is inadequate oxygen perfusion to the brain as a result of hypoxia or hypoperfusion. The undamaged brain tolerates low PaO2 levels better than the severely injured brain. Traumatized brain tissues are very sensitive to even moderate hypoxia (90 mm Hg). Gordon and Ponten proposed 2 explanations for this phenomenon: (1) Respiratory alkalosis may shift the oxygen-hemoglobin curve to the left, thereby increasing the affinity of the hemoglobin to the oxygen and decreasing the ease of oxygen release, and (2) uneven cerebral blood flow (CBF) may result from focal vasospasm with loss of focal autoregulation in the area of injured brain tissue.
[26] Approximately one third of patients with severe head injuries have been demonstrated to experience ischemic levels of CBF.
[30]

CBF is normally kept constant over a range (about 50-150 mm Hg) of cerebral perfusion pressure, as depicted in the image below. This is made possible by adjustments in vascular tone known as autoregulation (solid line). In patients with brain trauma, this autoregulation may malfunction, and CBF may become dependent on the CPP (dashed lines). Autoregulation is absent, diminished, or delayed in 50% of patients with severe head injuries.
[30] The lowest CBF values occur within the first 6-12 hours after injury.
[31, 32, 33, 34] The overall outcome of patients who experience ischemia is much worse than that of initially nonischemic patients.
[30, 35, 36] The initial ischemia is thought to cause permanent irreversible damage even if CBF is eventually optimized. The use of Xenon CT scan to measure CBF is now part of the armamentarium to diagnose and treat abnormalities in the CBF.

Brain edema is another form of secondary injury that may lead to elevated ICP and frequently results in increased mortality. Brain edema is categorized into 2 major types: vasogenic and cellular (or cytotoxic) edema.

Vasogenic edema occurs when a breach in the blood-brain barrier allows water and solutes to diffuse into the brain. Most of this fluid accumulates in the white matter and can be observed on head CT scans as hypodense white matter (on T1-weighted images) or as a bright signal area on the T2-weighted MRI. The mechanism of cellular (cytotoxic) edema is less clear. Theories include the increased uptake of extracellular potassium by the injured brain cells or the transport of HCO3- and H+ for Cl- and Na+ by the injured brain tissue as the mechanism of insult.
[26]

In one study, diffusion-weighted MR imaging was used to evaluate the apparent diffusion coefficient (ADC) in 44 patients with TBI (GCS < 8) and in 8 healthy volunteers. Higher ADC values have been associated with vasogenic edema, and lower ADC values have been associated with a predominantly cellular form of edema. Regional measurements of ADC in patients with focal and diffuse injury were computed. The final conclusion was that the brain swelling observed in patients with TBI appears to be predominantly cellular, as signaled by low ADC values in brain tissue with high levels of water content.
[37]

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Epidemiology

The incidence of closed head injury is estimated to be approximately 200 cases per 100,000 persons per year.
[2, 3, 4, 5, 6, 7]

Traumatic injuries remain the leading cause of death in children and in adults aged 45 years or younger.

The incidence varies by age, but children and young people experience closed head trauma more often than older populations.

Aggarwal S. Time course of cerebral flow and metabolic changes following severe head injury. Presented at: The 61st Annual Meeting of the American Association of Neurological Surgeons. Boston, Mass:. April 1993.